Effects of fluoride on microtubule ultrastructure and expression of Tubα1a and Tubβ2a in mouse hippocampus

Niu, Ruiyan; Xue, Xingchen; Yu-hong, Zhao; Sun, Zilong; Yan, Xiaoyan; Li, Xuying; Feng, Cuiping; Wang, Jundong

doi:10.1016/j.chemosphere.2015.07.011

Cited by 32 publications

(13 citation statements)

References 31 publications

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“…Of the received fluorine, 75 %–90 % undergoes absorption in the stomach and intestines, and 99 % of the fluorine that gets to the circulatory system is transported to tissues rich in calcium (mainly to hard tissues). Retrospective studies showed that the symptoms of fluorosis (the disorder of the physiology of bones and teeth and the damage to soft tissue) appeared when the supply of fluorine was over 0.15 mg/kg/24 h [2, 3, 6–9]. In recent years, scientists have been focusing on the toxic influence of this element on the nervous system.…”

Section: Introductionmentioning

confidence: 99%

“…The animals were exposed to high levels of fluorine (10, 25, 50 mg/L) for 8 months. The content of fluorides in the rats’ brains was even 250 times higher than in the control group [9]. However, the exact mechanisms by which fluorine decreases cognitive and learning abilities and causes memory loss were not clearly defined.…”

Section: Introductionmentioning

confidence: 99%

“…A proper construction of the cytoskeleton is important for the functioning of neurons. It was observed that the disorders in the construction of microtubules influence the deterioration of dendrites, the degeneration of axons and the decrease in the number of Purkinje cells [9, 19]. Among adult mice exposed to fluorine, a decrease in the expression of tubulins forming the heterodimers (Tuba1 and TubB2a) in the hippocampus was observed (the content of fluorine in drinking water, 100 mg/L).…”

Section: Introductionmentioning

confidence: 99%

“…Among adult mice exposed to fluorine, a decrease in the expression of tubulins forming the heterodimers (Tuba1 and TubB2a) in the hippocampus was observed (the content of fluorine in drinking water, 100 mg/L). The disorders in the synthesis of tubulins are important in relation to such processes as the maturing or the division of cells because they might lead to the creation of malfunctioning neurons without the ability of signal transmission [9]. …”

Section: Introductionmentioning

confidence: 99%

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The Influence of Fluorine on the Disturbances of Homeostasis in the Central Nervous System

Dec

Łukomska

Maciejewska

et al. 2016

Biol Trace Elem Res

121

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Fluorides occur naturally in the environment, the daily exposure of human organism to fluorine mainly depends on the intake of this element with drinking water and it is connected with the geographical region. In some countries, we can observe the endemic fluorosis—the damage of hard and soft tissues caused by the excessive intake of fluorine. Recent studies showed that fluorine is toxic to the central nervous system (CNS). There are several known mechanisms which lead to structural brain damage caused by the excessive intake of fluorine. This element is able to cross the blood-brain barrier, and it accumulates in neurons affecting cytological changes, cell activity and ion transport (e.g. chlorine transport). Additionally, fluorine changes the concentration of non-enzymatic advanced glycation end products (AGEs), the metabolism of neurotransmitters (influencing mainly glutamatergic neurotransmission) and the energy metabolism of neurons by the impaired glucose transporter—GLUT1. It can also change activity and lead to dysfunction of important proteins which are part of the respiratory chain. Fluorine also affects oxidative stress, glial activation and inflammation in the CNS which leads to neurodegeneration. All of those changes lead to abnormal cell differentiation and the activation of apoptosis through the changes in the expression of neural cell adhesion molecules (NCAM), glial fibrillary acidic protein (GFAP), brain-derived neurotrophic factor (BDNF) and MAP kinases. Excessive exposure to this element can cause harmful effects such as permanent damage of all brain structures, impaired learning ability, memory dysfunction and behavioural problems. This paper provides an overview of the fluoride neurotoxicity in juveniles and adults.

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Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

The Influence of Fluorine on the Disturbances of Homeostasis in the Central Nervous System

Dec

Łukomska

Maciejewska

et al. 2016

Biol Trace Elem Res

121

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“…Group 4 was given drinking water containing NaF (100 mg/L) and intragastrically administrated GSPE (400 mg/kg body weight). These dosages were chosen on the basis of previous studies (Zhou et al, 2015;Niu et al, 2015). All of the mice were treated daily for 5 weeks.…”

Section: Animals and Treatmentmentioning

confidence: 99%

Fluoride-induced iron overload contributes to hepatic oxidative damage in mouse and the protective role of Grape seed proanthocyanidin extract

Niu

He²,

et al. 2018

J. Toxicol. Sci.

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-Emerging evidence has demonstrated that iron overload plays an important role in oxidative stress in the liver. This study aimed to explore whether fluoride-induced hepatic oxidative stress is associated with iron overload and whether grape seed proanthocyanidin extract (GSPE) alleviates oxidative stress by reducing iron overload. Forty Kunming male mice were randomly divided into 4 groups and treated for 5 weeks with distilled water (control), sodium fluoride (NaF) (100 mg/L), GSPE (400 mg/kg bw), or NaF (100 mg/L) + GSPE (400 mg/kg bw). Mice exposed to NaF showed typical poisoning changes of morphology, increased aspartate aminotransferase and alanine aminotransferase activities in the liver. NaF treatment also increased MDA accumulation, decreased GSH-Px, SOD and T-AOC levels in liver, indicative of oxidative stress. Intriguingly, all these detrimental effects were alleviated by GSPE. Further study revealed that NaF induced disorders of iron metabolism, as manifested by elevated iron level with increased hepcidin but decreased ferroportin expression, which contributed to hepatic oxidative stress. Importantly, the iron dysregulation induced by NaF could be normalized by GSPE. Collectively, these data provide a novel insight into mechanisms underlying fluorosis and highlight the potential of GSPE as a naturally occurring prophylactic treatment for fluoride-induced hepatotoxicity associated with iron overload.

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Principles of fluoride toxicity and the cellular response: a review

2020

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Effects of fluoride on microtubule ultrastructure and expression of Tubα1a and Tubβ2a in mouse hippocampus

Cited by 32 publications

References 31 publications

The Influence of Fluorine on the Disturbances of Homeostasis in the Central Nervous System

The Influence of Fluorine on the Disturbances of Homeostasis in the Central Nervous System

Fluoride-induced iron overload contributes to hepatic oxidative damage in mouse and the protective role of Grape seed proanthocyanidin extract

Principles of fluoride toxicity and the cellular response: a review

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